@article{10902/38612,
year = {2025},
url = {https://hdl.handle.net/10902/38612},
abstract = {Centriole and/or cilium defects are characteristic of cancer cells and have been linked to cancer cell invasion. However, the mechanistic bases of this regulation remain incompletely understood. Spindle assembly abnormal protein 6 homolog (SAS-6) is essential for centriole biogenesis and cilium formation. SAS-6 levels decrease at the end of mitosis and G1, resulting from APCCdh1-targeted degradation. To examine the biological consequences of unrestrained SAS-6 expression, we used a nondegradable SAS-6 mutant (SAS-6ND). This led to an increase in ciliation and cell invasion and caused an up-regulation of the YAP/TAZ pathway. SAS-6ND expression resulted in cell morphology changes, nuclear deformation, and YAP translocation to the nucleus, resulting in increased TEAD-dependent transcription. SAS-6-mediated invasion was prevented by YAP down-regulation or by blocking ciliogenesis. Similarly, down-regulation of SAS-6 in DMS273, a highly invasive and highly ciliated lung cancer cell line that overexpresses SAS-6, completely blocked cell invasion and depleted YAP protein levels. Thus, our data provide evidence for a defined role of SAS-6 in cell invasion through the activation of the YAP/TAZ pathway.},
publisher = {Life Science Alliance, LLC},
publisher = {Life Science Alliance, 2026, 8(10), e202402820},
title = {Dysregulated SASS6 expression promotes increased ciliogenesis and cell invasion phenotypes},
author = {Hargreaves, Eleanor and Collinson, Rebecca and Jenks, Andrew D. and Staszewski, Adina and Tsalikis, Athanasios and Bodoque, Raquel and Arias-García, Mar and Abdi, Yasmin and Al-Malki, Abdulaziz and Yuan, Yinyin and Natrajan, Rachael and Haider, Syed and Iskratsch, Thomas and Wang, Won-Jing and Goinho, Susana and Palaskas, Nicolaos J. and Calvo González, Fernando and Vivanco, Igor and Zech, Tobias and Tanos, Barbara E.},
}